Shock can be defined as acute circulatory failure leading to inadequate tissue perfusion causing cellular hypoxia. This leads to cellular disorder and failure of multiple organs. Hypotension can be thought to be synonymous with shock but occasionally cellular perfusion can be inadequate despite a normal blood pressure.
Regardless of the underlying cause, shock leads to inadequate tissue perfusion with resultant cellular damage. Arterial blood pressure and therefore tissue perfusion is dependent on various factors (preload, contractility, afterload, heart rate and systemic vascular resistance); therefore a problem with any one of these factors can lead to a shocked state.
Shock can be categorised according to the underlying problem.
There are 4 principle categories of shock:
Alternatively, causes of shock can be categorised according to their effect on the preload, cardiac contractility and afterload:
Hypovolaemic shock is the most common cause of shock and is due to a decreased circulating volume and thus reduced preload. The reduced preload (volume returning to the heart) causes a reduced stroke volume and therefore reduced cardiac output. The body initially responds to this reduction in cardiac output by increasing the heart rate and systemic vascular resistance (due to circulating catecholamine released as part of the stress response). Therefore it is possible for a patient in hypovolaemic shock to maintain a relatively normal blood pressure in the early stages. Clinically the patient is peripherally shutdown and cool to touch. Common causes are dehydration, fluid loss and haemorrhage.
Septic shock is often a result of overwhelming infection, where inflammatory mediators stimulate peripheral blood vessels to dilate, resulting in a reduced SVR. A reduced SVR causes hypotension and inadequate end organ perfusion. In the early stages of septic shock the cardiac output is increased to compensate for the reduced SVR. This manifests clinically as a warm patient with bounding pulses, but as the sepsis progresses cardiac function deteriorates and the less common presentation of ‘cold’ septic shock becomes evident.
Anaphylactic shock, like septic shock results in inflammatory mediator-led peripheral vasodilation. Anaphylactic reactions are immunoglobulin E (IgE) antibody mediated causing massive degranulation of mast cells with histamine release. This results in severe vasodilatation, reduced SVR and cardiovascular collapse. This normally occurs very rapidly and in severe cases cardiac arrest will occur.
Cardiogenic shock refers to cardiac pump failure. This can be caused by acute damage (myocardial infarction), arrhythmias, or relative fluid overload on an already ineffective heart (heart failure). A reduction in cardiac contractility results in a reduced stroke volume and therefore cardiac output. SVR often increases as a compensatory measure.
Obstructive shock is caused by impairment of cardiac function due to an obstruction of the cardiac output. Causes include massive pulmonary emboli, cardiac tamponade or tension pneumothorax. For example, a tension pneumothorax increases intra-thoracic pressure to the extent that venous return to the heart is compromised. This is effectively a reduction in the preload and therefore leads to a reduced stroke volume and cardiac output.